Diabetic ketoacidosis (DKA) is a life-threatening acute metabolic disturbance that results from absolute or relative insulin deficiency. It is usually precipitated by intercurrent illness and is a relatively common complication of type 1 diabetes but only rarely occurs in those suffering type 2 diabetes. The cardinal features of DKA are hyperglycemia (blood glucose usually greater then 15.0 mmol/L and often much higher) with resulting glycosuria, metabolic acidosis (reduced arterial pH and bicarbonate) and ketosis (presence of ketones in blood and urine). Although moderate-to-severe hyperglycemia is an almost invariable finding in patients with DKA, there are rare reports of ketoacidosis occurring in diabetics with normal or near-normal blood glucose. The diagnosis of euglycemic diabetic ketoacidosis is applied to such patients and there is now consensus that blood glucose of less than 11.1 mmol/L (200 mg/dL) is required for such a diagnosis. A recently published case history describes DKA occurring in a patient with long-standing type 1 diabetes who presented with blood glucose of just 5.8 mmol/L (105 mg/dL). This must be one of the lowest, if not the lowest-ever blood glucose concentration to be recorded in a patient with untreated DKA. The case concerns a 39-year-old male whose type 1 diabetes had been diagnosed 19 years previously and who presented to the emergency room of his local hospital with a 4-day history of nausea, vomiting and flu-like symptoms. DKA was suspected and confirmed on blood and urine testing (pH 7.3, bicarbonate 10 mmol/L, heavy (4+) ketonuria). Gastroenteritis was presumed to be the precipitating factor. The diagnosis of euglycemic DKA was made when blood sampled at the same time revealed glucose concentration was 5.8 mmol/L. Glucose was absent from urine. Acidosis was successfully treated following hospital admission but the patient appeared to have no interest in food, and admitted to not having eaten for 2-3 weeks prior to hospitalization. Following psychiatric referral a diagnosis of severe depression was made and it was supposed that this had caused appetite suppression and starvation. Starvation ketoacidosis was considered a contributory factor in the development of DKA. The patient had reported increasing his insulin dose during the three days of illness prior to admission in accordance with medical advice. This no doubt helped protect from the hyperglycemia that is an almost invariable finding in DKA. In discussion of the case history the authors focused on the way starvation can contribute to ketoacidosis in the diabetic patient and the complexity of distinguishing starvation ketoacidosis from euglycemic DKA. They remind that normal blood glucose is not sufficient evidence to exclude life-threatening ketoacidosis.